Concordance and Discordance Between Brain Perfusion and Atrophy in Frontotemporal Dementia

Shimizu, Soichiro; Laxamana, Joel; Miller, Bruce L.; Kramer, Joel H.; Weiner, Michael W.; Schuff, Norbert

doi:10.1007/s11682-009-9084-1

Cited by 27 publications

(56 citation statements)

References 35 publications

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“…While much of our findings resemble SPECT-based observations in dementia (Matsuda et al, 2002; Matsuda et al, 2003) and more recently using CASL (Dai et al, 2009; Hayasaka et al, 2006; Nagata et al, 2000; Schuff et al, 2009; Shimizu et al, 2010; Yang et al, 2002) and AD (Tosun et al, 2010), some exceptions were found, such as in the amygdala (Dai et al, 2009) and hippocampus (Alsop et al, 2008; Dai et al, 2009; Fleisher et al, 2009; Heo et al, 2010; Ito et al, 2006; Nagata et al, 2000). …”

Section: Discussionsupporting

confidence: 88%

Age-associated reductions in cerebral blood flow are independent from regional atrophy

2011

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Prior studies have demonstrated decreasing cerebral blood flow (CBF) in normal aging, but the full spatial pattern and potential mechanism of changes in CBF remain to be elucidated. Specifically, existing data have not been entirely consistent regarding the spatial distribution of such changes, potentially a result of neglecting the effect of age-related tissue atrophy in CBF measurements. In this work, we use pulsed arterial-spin labelling to quantify regional CBF in 86 cognitively and physically healthy adults, aged 23 to 88 years. Surface-based analyses were utilized to map regional decline in CBF and cortical thickness with advancing age, and to examine the spatial associations and dissociations between these metrics. Our results demonstrate regionally selective age-related reductions in cortical perfusion, involving the superior-frontal, orbito-frontal, superior-parietal, middle-inferior temporal, insular, precuneus, supramarginal, lateral-occipital and cingulate regions, while subcortical CBF was relatively preserved in aging. Regional effects of age on CBF differed from that of grey-matter atrophy. In addition, the pattern of CBF associations with age displays an interesting similarity with the default-mode network. These findings demonstrate the dissociation between regional CBF and structural alterations specific to normal aging, and augment our understanding of mechanisms of pathology in older adults.

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Section: Discussionsupporting

confidence: 88%

Age-associated reductions in cerebral blood flow are independent from regional atrophy

2011

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“…Our first finding with multimodality jICA extends our earlier MRI findings of partially dissociated structural and physiological alteration in behavioral variant frontotemporal dementia based on simply combining the statistics from structural and perfusion MRI (Shimizu et al, 2010). The observed dissociations involved substantial atrophy in absence of rCBF* reduction in some brain regions in behavioral variant frontotemporal dementia while other brain regions showed concordant levels of atrophy and rCBF* reductions.…”

Section: Discussionsupporting

confidence: 80%

“…Furthermore, to identify regions of concordance and discordance between structural and physiological brain changes in neurodegenerative diseases without explicitly modeling the relationships, we developed functions to combine the statistics from different MRI modalities (Hayasaka et al, 2006). We recently applied this approach to study regional dissociations between brain atrophy and reduced rCBF in FTD, showing regionally varying reduction in rCBF despite widespread tissue atrophy (Shimizu et al, 2010). Moreover, to determine the added value of perfusion-weighted MRI beyond the value of structural MRI for the correct classification of AD, we performed cortical point-by-point tests based on logistic regressions to identify the regions where largely atrophy contributed to the classification and regions where reduced rCBF alone or in conjunction with atrophy made contributions (Tosun et al, 2010).…”

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confidence: 99%

“…We choose behavioral variant frontotemporal dementia for this test, because previous imaging studies have implicated a signature pattern for each regional brain atrophy and rCBF deficits in patients with behavioral variant frontotemporal dementia (Cardenas et al, 2007; Chao et al, 2007; Du et al, 2006; Grimmer et al, 2004; Grossman et al, 2004; Ishii et al, 1998; Jeong et al, 2005; Nagao et al, 2004; Rosen et al, 2002; Varrone et al, 2002; Whitwell et al, 2005). These atrophy and rCBF patterns in behavioral variant frontotemporal dementia overlap partially but are also distinctly discordant (Shimizu et al, 2010) and therefore exhibit an attractive level of complexity to test if jICA can reveal large scale associations between alterations in structure and physiology across the brain in behavioral variant frontotemporal dementia. The specific objective of this study was twofold: (1) to determine the extent to which brain regions in behavioral variant frontotemporal dementia with greater atrophy than in controls are also associated with which brain regions with greater rCBF reduction using multimodality jICA and (2) to test if the brain regions identified by multimodality jICA provide a better discrimination between behavioral variant frontotemporal dementia patients and controls (i.e., effect size) than the regions identified by conventional unimodality analyses of structural and perfusion-weighted MRI data separately.…”

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confidence: 99%

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MRI patterns of atrophy and hypoperfusion associations across brain regions in frontotemporal dementia

et al. 2012

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Magnetic Resonance Imaging (MRI) provides various imaging modes to study the brain. We tested the benefits of a joint analysis of multimodality MRI data in combination with a large-scale analysis that involved simultaneously all image voxels using joint independent components analysis (jICA) and compared the outcome to results using conventional voxel-by-voxel unimodality tests. Specifically, we designed a jICA to decompose multimodality MRI data into independent components that explain joint variations between the image modalities as well as variations across brain regions. We tested the jICA design on structural and perfusion-weighted MRI data from 12 patients diagnosed with behavioral variant frontotemporal dementia (bvFTD) and 12 cognitively normal elderly individuals. While unimodality analyses showed widespread brain atrophy and hypoperfusion in the patients, jICA further revealed two significant joint components of variations between atrophy and hypoperfusion across brain regions. The 1st joint component revealed associated brain atrophy and hypoperfusion predominantly in the right brain hemisphere in behavioral variant frontotemporal dementia, and the 2nd joint component revealed greater atrophy relative to hypoperfusion affecting predominantly the left hemisphere in behavioral variant frontotemporal dementia. The patterns are consistent with the clinical symptoms of behavioral variant frontotemporal dementia that relate to asymmetric compromises of the left and right brain hemispheres. The joint components also revealed that that structural alterations can be associated with physiological alterations in spatially separated but potentially connected brain regions. Finally, jICA outperformed voxel-by-voxel unimodal tests significantly in terms of an effect size, separating the behavioral variant frontotemporal dementia patients from the controls. Taken together, the results demonstrate the benefit of multimodality MRI in conjunction with jICA for mapping neurodegeneration, which may lead ultimately to an improved diagnosis of behavioral variant frontotemporal dementia and other forms of neurodegenerative diseases.

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“…; Shimizu et al . ). The presence of posterior cingulate hypoperfusion has recently been shown to be a sensitive early stage differential diagnostic marker in separating AD from bvFTD (Steketee et al .…”

Section: Neuroanatomical Signatures Of Ftdmentioning

confidence: 97%

Advances in neuroimaging in frontotemporal dementia

Gordón

Rohrer

Fox

2016

Journal of Neurochemistry

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Frontotemporal dementia (FTD) is a clinically and neuroanatomically heterogeneous neurodegenerative disorder with multiple underlying genetic and pathological causes. Whilst initial neuroimaging studies highlighted the presence of frontal and temporal lobe atrophy or hypometabolism as the unifying feature in patients with FTD, more detailed studies have revealed diverse patterns across individuals, with variable frontal or temporal predominance, differing degrees of asymmetry, and the involvement of other cortical areas including the insula and cingulate, as well as subcortical structures such as the basal ganglia and thalamus. Recent advances in novel imaging modalities including diffusion tensor imaging, resting-state functional magnetic resonance imaging and molecular positron emission tomography imaging allow the possibility of investigating alterations in structural and functional connectivity and the visualisation of pathological protein deposition. This review will cover the major imaging modalities currently used in research and clinical practice, focusing on the key insights they have provided into FTD, including the onset and evolution of pathological changes and also importantly their utility as biomarkers for disease detection and staging, differential diagnosis and measurement of disease progression. Validating neuroimaging biomarkers that are able to accomplish these tasks will be crucial for the ultimate goal of powering upcoming clinical trials by correctly stratifying patient enrolment and providing sensitive markers for evaluating the effects and efficacy of diseasemodifying therapies.

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Concordance and Discordance Between Brain Perfusion and Atrophy in Frontotemporal Dementia

Cited by 27 publications

References 35 publications

Age-associated reductions in cerebral blood flow are independent from regional atrophy

Age-associated reductions in cerebral blood flow are independent from regional atrophy

MRI patterns of atrophy and hypoperfusion associations across brain regions in frontotemporal dementia

Advances in neuroimaging in frontotemporal dementia

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